Biological Causes of Eating Disorders

Biological  Causes of Eating Disorders

“Epigenetic mechanisms contribute to the known alterations of ANP homeostasis in  eating disorders.”

Eating disorders refer to a group of conditions defined by abnormal eating habits that may involve either insufficient or excessive food intake to the detriment of an individual’s physical and mental health. Bulimia nervosa, anorexia nervosa, and binge eating disorder are the most common specific forms in the United Kingdom.Though primarily thought of as affecting females eating disorders affect males as well. An estimated 10 – 15% of people with eating disorders are males. Although eating disorders are increasing all over the world among both men and women, there is evidence to suggest that it is women in the Western world who are at the highest risk of developing them and the degree of westernization increases the risk. Nearly half of all Americans personally know someone with an eating disorder. The skill to comprehend the central processes of appetite has increased tremendously since leptin was discovered, and the skill to observe the functions of the brain as well.

The precise cause of eating disorders is not entirely understood, but there is evidence that it may be linked to other medical conditions and situations. Cultural idealization of thinness and youthfulness have contributed to eating disorders affecting diverse populations. One study showed that girls with ADHD have a greater chance of getting an eating disorder than those not affected by ADHD.Another study suggested that women with PTSD, especially due to sexually related trauma, are more likely to develop anorexia nervosa.One study showed that foster girls are more likely to develop bulimia nervosa. Some think that peer pressure and idealized body-types seen in the media are also a significant factor. Some research show that for certain people there are genetic reasons why they may be prone to developing an eating disorder.

While proper treatment can be highly effective for many suffering from specific types of eating disorders, the consequences of eating disorders can be severe, including death(whether from direct medical effects of disturbed eating habits or from comorbid conditions such as suicidal thinking

The specific cause/ causes of eating disorders are unknown. However, it is believed to be due to a combination of biological, psychological and/or environmental abnormalities. A common belief is that “Genetics loads the gun, environment pulls the trigger. This would mean that some people are born with a predisposition to it, which can be brought to the surface pending on environment and reactions to it. Many people with eating disorders suffer also from body dysmorphic disorder, altering the way a person sees themselves.There are also many other possibilities such as environmental, social and interpersonal issues that could promote and sustain this illness.Also, the media are oftentimes blamed for the rise in the incidence of eating disorders due to the fact that media images of idealized slim physical shape of people such as models and celebrities motivate or even force people to attempt to achieve slimness themselves. The media are accused of distorting reality, in the sense that people portrayed in the media are either naturally thin and thus unrepresentative of normality or unnaturally thin by forcing their bodies to look like the ideal image by putting excessive pressure on themselves to look a certain way.

Biological  Causes of Eating Disorders

  • Genetic: Numerous studies have been undertaken that show a possible genetic predisposition toward eating disorders as a result of Mendelian inheritance.[24][24][25]
  • Epigenetics: Epigenetic mechanisms are means by which environmental effects alter gene expression via methods such as DNA methylation; these are independent of and do not alter the underlying DNA sequence. They are heritable, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission due to epigenetic mechanisms has been implicated in various eating disorders.
  • Biochemical: Eating behavior is a complex process controlled by the neuroendocrine system of which the Hypothalamus-pituitary-adrenal-axis (HPA axis) is a major component. Dysregulation of the HPA axis has been associated with eating disorders,such as irregularities in the manufacture, amount or transmission of certain neurotransmitters, hormonesor neuropeptidesand amino acids such as homocysteine, elevated levels of which are found in AN and BN as well as depression.
    • serotonin: a neurotransmitter involved in depression also has an inhibitory effect on eating behavior
    • norepinephrine is both a neurotransmitter and a hormone; abnormalities in either capacity may affect eating behavior
    • dopamine: which in addition to being a precursor of norepinephrine and epinephrine is also a neurotransmitter which regulates the rewarding property of food
  • leptin and ghrelin: leptin is a hormone produced primarily by the fat cells in the body; it has an inhibitory effect on appetite by inducing a feeling of saiety. Ghrelin is an appetite inducing hormone produced in the stomach and the upper portion of the small intestine. Circulating levels of both hormones are an important factor in weight control. While often associated with obesity, both hormones and their respective effects have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.
  • immune system: studies have shown that a majority of patients with anorexia and bulimia nervosa have elevated levels of autoantibodies that affect hormones and neuropeptides that regulate appetite control and the stress response. There may be a direct correlation between autoantibody levels and associated psychological traits.
  • infection: PANDAS, is an abbreviation for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections. Children with PANDAS “have obsessive-compulsive disorder (OCD) and/or tic disorders such as Tourette syndrome, and in whom symptoms worsen following infections such as “strep throat” and scarlet fever.” (NIMH) There is a possibility that PANDAS may be a precipitating factor in the development of anorexia nervosa in some cases, (PANDAS AN
  • lesions: studies have shown that lesions to the right frontal lobe or temporal lobe can cause the pathological symptoms of an eating disorder
  • tumors: tumors in various regions of the brain have been implicated in the development of abnormal eating patterns
  • brain calcification: a study highlights a case in which prior calcification of the right thalumus may have contributed to development of anorexia nervosa
  • somatosensory homunculus: is the representation of the body located in the somatosensory cortex, first described by renowned neurosurgeon Wilder Penfield. The illustration was originally termed “Penfield’s Homunculus”, homunculus meaning little man. “In normal development this representation should adapt as the body goes through its pubertal growth spurt. However, in AN it is hypothesized that there is a lack of plasticity in this area, which may result in impairments of sensory processing and distortion of body image”. (Bryan Lask, also proposed by VS Ramachandran)
  • Obstetric complications: There have been studies done which show maternal smoking, obstetric and perinatal complications such as maternal anemia, very pre-term birth (32<wks.), being born small for gestational age, neonatal cardiac problems, preeclampsia, placental infarction and sustaining a cephalhematoma at birth increase the risk factor for developing either anorexia nervosa or bulimia nervosa. Some of this developmental risk as in the case of placental infarction, maternal anemia and cardiac problems may cause intrauterine hypoxia, umbilical cord occlusion or cord prolapse may cause ischemia, resulting in cerebral injury, the prefrontal cortex in the fetus and neonate is highly susceptible to damage as a result of oxygen deprivation which has been shown to contribute to executive dysfunction, ADHD, and may affect personality traits associated with both eating disorders and comorbid disorders such as impulsivity, mental rigidity and obsessionality. The problem of perinatal brain injury, in terms of the costs to society and to the affected individuals and their families, is extraordinary.

Psychological

Eating disorders are classified as Axis I disorders in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV) published by the American Psychiatric Association. There are various other psychological issues that may factor into eating disorders, some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Axis II disorders are subtyped into 3 “clusters”: A, B and C. The causality between personality disorders and eating disorders has yet to be fully established.Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.Some develop them afterwards.The severity and type of eating disorder symptoms have been shown to affect comorbidity.The DSM-IV should not be used by laypersons to diagnose themselves, even when used by professionals there has been considerable controversy over the diagnostic criteria used for various diagnoses, including eating disorders. There has been controversy over various editions of the DSM including the latest edition, DSM-V, due in May 2013

References:

  • Patrick, L (2002). “Eating disorders: a review of the literature with emphasis on medical complications and clinical nutrition”. Alternative medicine review : a journal of clinical therapeutic 7 (3): 184–202.
  • Frieling, H; Römer, KD; Scholz, S; Mittelbach, F; Wilhelm, J; De Zwaan, M; Jacoby, GE; Kornhuber, J et al. (2010). “Epigenetic dysregulation of dopaminergic genes in eating disorders”. The International Journal of Eating Disorders 43 (7): 577–83. .
  • Frieling, H; Bleich, S; Otten, J; Römer, KD; Kornhuber, J; De Zwaan, M; Jacoby, GE; Wilhelm, J et al. (2008). “Epigenetic downregulation of atrial natriuretic peptide but not vasopressin mRNA expression in females with eating disorders is related to impulsivity”. Neuropsychopharmacology 33 (11): 2605–9.
  • Gross, MJ; Kahn, JP; Laxenaire, M; Nicolas, JP; Burlet, C (1994). “Corticotropin-releasing factor and anorexia nervosa: reactions of the hypothalamus-pituitary-adrenal axis to neurotropic stress”. Annales d’endocrinologie 55 (6): 221–8.
  • Licinio, J; Wong, ML; Gold, PW (1996). “The hypothalamic-pituitary-adrenal axis in anorexia nervosa”. Psychiatry Research 62 (1): 75–83.
  • Chaudhri, O; Small, C; Bloom, S (2006). “Gastrointestinal hormones regulating appetite”. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 361 (1471): 1187–209.
  • ^ Gendall, KA; Kaye, WH; Altemus, M; McConaha, CW; La Via, MC (1999). “Leptin, neuropeptide Y, and peptide YY in long-term recovered eating disorder patients”. Biological Psychiatry 46 (2): 292–9.
  • Wilhelm, J; Müller, E; De Zwaan, M; Fischer, J; Hillemacher, T; Kornhuber, J; Bleich, S; Frieling, H (2010). “Elevation of homocysteine levels is only partially reversed after therapy in females with eating disorders”. Journal of neural transmission (Vienna, Austria : 1996) 117 (4): 521–7.
  • Jimerson, DC; Lesem, MD; Kaye, WH; Hegg, AP; Brewerton, TD (1990). “Eating disorders and depression: is there a serotonin connection?”. Biological Psychiatry 28 (5): 443–54.

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